The proposed research is designed to examine the significance of identifiable biochemical aberrations of abnormal polymorphonuclear leukocyte function in patients with major thermal trauma, to document the relationship of leukocyte dysfunction to sepsis in these patients, and to establish the role of such PMN dysfunction in non-burn trauma. The contribution of both oxidative and non-oxidative mechanisms to this important host defense system will be examined. Serial measurements of NBT reduction, O2 consumption, NAD(P)H oxidase activity, O minus 2., superoxide dismutase, H2O2 and myeloperoxidase activity will be performed in thermally injured and non-burn trauma patients as well as in normal controls. In addition, the roles of glutathione reductase glutathione peroxidase, catalase and glucose-6-phosphate dehydrogenase will be examined. Circulating mediators of defective leukocyte function will be sought. Identification of these abnormalities and determination of the responsible agents should provide better preventive and/or corrective treatment regimens for these patients.